EpCAM-Independent Enrichment of Circulating Tumor Cells in Metastatic Breast Cancer.
Düsseldorf, Germany. In Plos One, 2014
The expression of respective proteins (Trop2, CD49f, c-Met, CK8, CD44, ADAM8, CD146, TEM8, CD47) was verified by immunofluorescence on EpCAMpos (e.g.
Alemtuzumab in the treatment of multiple sclerosis.
Málaga, Spain. In J Inflamm Res, 2013
Approval was granted on the strength of two pivotal studies, Comparison of Alemtuzumab and Rebif® Efficacy in Multiple Sclerosis (CARE-MS)-1 in the first-line setting and CARE-MS-2 in patients who had failed first-line therapy.
ADAM8 in asthma. Friend or foe to airway inflammation?
Chongqing, China. In Am J Respir Cell Mol Biol, 2013
Recruitment of leukocytes from the vasculature into airway sites is essential for induction of airway inflammation, a process thought to be mediated by a disintegrin and metalloprotease 8 (ADAM8).
α-Cleavage of cellular prion protein.
Cleveland, United States. In Prion, 2012
We demonstrated that, in muscle cells, ADAM8 is the primary protease for the α-cleavage of PrP (C) , but another unidentified protease(s) must also play a minor role.
ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23.
New York City, United States. In Nat Immunol, 2006
Here we used loss-of-function and gain-of-function experiments with cells lacking or overexpressing candidate CD23-releasing enzymes (ADAM8, ADAM9, ADAM10, ADAM12, ADAM15, ADAM17, ADAM19 and ADAM33), ADAM-knockout mice and a selective inhibitor to identify ADAM10 as the main CD23-releasing enzyme in vivo.